Upregulation of inflammatory mediators in end-stage renal disease as measured using biochip array technology.

Systemic vascular changes contribute to both the pathogenesis and thrombotic comorbidities of end-stage renal disease (ESRD). This study aims to profile various biomarkers and better understand their role in the pathogenesis of ESRD. Plasma samples from 49 patients with ESRD and 56 control individuals were analyzed for markers for inflammation, specifically C-reactive protein (CRP), tumor necrosis factor receptor 1 (TNFR1), neutrophil gelatinase-associated lipocalin (NGAL); thrombomodulin (TM); neuron-specific enolase (NSE), and thrombosis-D-dimer (DD). Compared to controls, all markers studied showed a statistically significant upregulation in patients with ESRD. These results indicate a polypathologic process in patients with ESRD, leading to cardiovascular and cerebrovascular events. However, the clinical significance of previously untested markers, such as TNFR1, NGAL, and NSE, still needs to be further explored. This study further validates the role of endothelial damage and endogenous thrombotic processes in ESRD as evidenced by the increased levels of TM and DD.